Rare but Revealing: Gallbladder Agenesis in Dogs Unveiled Through CT and Laparoscopy

Gallbladder Agenesis in 17 Dogs: 2006–2016

K. Sato, M. Sakai, S. Hayakawa, Y. Sakamoto, Y. Kagawa, K. Kutara, K. Teshima, K. Asano, T. Watar

Background:
Gallbladder agenesis (GBA) is an extremely rare congenital condition in dogs, characterized by the absence of the gallbladder without extrahepatic biliary atresia. While GBA in humans is often asymptomatic and incidentally diagnosed, dogs may present with signs of hepatobiliary disease. Previous canine reports are limited to isolated cases. This study aimed to describe the clinical characteristics, diagnostic approaches, treatment, and outcomes in a larger cohort of dogs diagnosed with GBA.

Methods:
This retrospective study reviewed medical records from 2006 to 2016 at a veterinary medical center. Seventeen dogs were included based on suspected GBA on abdominal ultrasonography, confirmed by gross evaluation during laparoscopy or laparotomy. Data collected included signalment, clinical signs, laboratory values, imaging findings, histopathology, treatments, and outcomes. Computed tomography (CT) cholangiography and portography were employed to assess biliary anatomy and detect portosystemic shunts. Liver biopsy samples were analyzed histologically to identify ductal plate malformation (DPM).

Results:
Most dogs were young small-breed dogs, especially Chihuahuas. Clinical signs were variable; vomiting was most common, though nearly half were asymptomatic. All dogs had elevated liver enzyme activity, especially ALT. CT cholangiography revealed common bile duct (CBD) dilation in 12 of 15 dogs, with no obstruction. Gross liver abnormalities were seen in 14 of 17 dogs. Histologically, 16 of 17 dogs were diagnosed with DPM, with findings such as portal vein narrowing, bile duct profile increase, and portal fibrosis. One dog died shortly after diagnosis due to severe ascites. At follow-up, 16 dogs were alive, though some had signs of progressive liver dysfunction.

Limitations:
The study's retrospective design and small sample size limit the generalizability of findings. Diagnostic criteria for DPM versus primary hypoplasia of the portal vein are overlapping and remain a subject of debate. Genetic studies were not performed, and no longitudinal biopsies were taken to assess histological progression. Breed predisposition could not be definitively determined due to lack of population data.

Conclusions:
GBA in dogs is associated with congenital malformations of the liver and intrahepatic biliary structures, frequently leading to elevated liver enzymes and histologic evidence of DPM. CT cholangiography was more sensitive than ultrasound in identifying non-obstructive CBD dilation and is recommended alongside laparoscopy for definitive diagnosis. Regular follow-up is warranted due to the potential for progressive liver dysfunction and portal hypertension. Further genetic and long-term outcome studies are needed.

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